Thyroid's secretory capacity

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Thyroid's secretory capacity
Medical diagnostics
Reference range 1.41–8.67 pmol/s
LOINC 82368-2

Thyroid's secretory capacity (GT, also referred to as thyroid's incretory capacity, maximum thyroid hormone output, T4 output or, if calculated from levels of thyroid hormones, as SPINA-GT) is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit (e.g. one second).[1] [2]

How to determine GT[edit]

Experimentally, GT can be determined by stimulating the thyroid with a high thyrotropin concentration (e.g. by means of rhTSH, i.e. recombinant human thyrotropin) and measuring its output in terms of T4 production, or by measuring the serum concentration of protein-bound 131I after administration of radioiodine.[3]

In vivo, GT can also be estimated from equilibrium levels of TSH and T4 or free T4. In this case it is calculated with

or

: Theoretical (apparent) secretory capacity (SPINA-GT)
: Dilution factor for T4 (reciprocal of apparent volume of distribution, 0.1 l−1)
: Clearance exponent for T4 (1.1e-6 sec−1)
K41: Dissociation constant T4-TBG (2e10 l/mol)
K42: Dissociation constant T4-TBPA (2e8 l/mol)
DT: EC50 for TSH (2.75 mU/l)[1][4]

The ratio of SPINA-GT and thyroid volume (as determined by ultrasonography) is referred to as specific thyroid capacity (SPINA-GTs).

Reference Range[edit]

Lower limit Upper limit Unit
1.41[1] 8.67[1] pmol/s

The equations and their parameters are calibrated for adult humans with a body mass of 70 kg and a plasma volume of ca. 2.5 l.[1]

Clinical significance[edit]

SPINA-GT is elevated in primary hyperthyroidism and reduced in primary hypothyroidism,[5][6][7] and it has been observed to correlate with thyroid volume.[1] In longitudinal evaluation GT shows lower intraindividual variation (i.e. higher reliability) than TSH, FT4 or FT3.[8]

Correlation of SPINA-GT with creatinine clearance suggested a negative influence of uremic toxins on thyroid biology.[9] In the initial phase of major non-thyroidal illness SPINA-GT may be temporarily elevated.[10]

Specific secretory capacity (SPINA-GTs) is reduced in obesity[1] and autoimmune thyroiditis.[11][12]

See also[edit]

External links[edit]

References[edit]

  1. ^ a b c d e f g Dietrich, J. W. (2002). Der Hypophysen-Schilddrüsen-Regelkreis. Berlin, Germany: Logos-Verlag Berlin. ISBN 978-3-89722-850-4. OCLC 50451543. 3897228505 
  2. ^ Dietrich, Johannes W.; Landgrafe-Mende, Gabi; Wiora, Evelin; Chatzitomaris, Apostolos; Klein, Harald H.; Midgley, John E. M.; Hoermann, Rudolf (9 June 2016). "Calculated Parameters of Thyroid Homeostasis: Emerging Tools for Differential Diagnosis and Clinical Research". Frontiers in Endocrinology. 7. doi:10.3389/fendo.2016.00057. PMC 4899439Freely accessible. PMID 27375554. 
  3. ^ Bierich, J. R. (1964). Endokrinologie. In: H. Wiesener: Einführung in die Entwicklungsphysiologie des Kindes. [S.l.]: Springer. p. 310. ISBN 978-3-642-86507-7. 
  4. ^ Dietrich JW, Stachon A, Antic B, Klein HH, Hering S (Oct 2008). "The AQUA-FONTIS study: protocol of a multidisciplinary, cross-sectional and prospective longitudinal study for developing standardized diagnostics and classification of non-thyroidal illness syndrome". BMC Endocr Disord. 8 (1): 13. doi:10.1186/1472-6823-8-13. PMC 2576461Freely accessible. PMID 18851740. 
  5. ^ Dietrich, J., M. Fischer, J. Jauch, E. Pantke, R. Gärtner und C. R. Pickardt (1999). "SPINA-THYR: A Novel Systems Theoretic Approach to Determine the Secretion Capacity of the Thyroid Gland." European Journal of Internal Medicine 1999; 10(Suppl. 1): S34.
  6. ^ Dietrich JW (Sep 2012). "Thyroid storm". Med Klin Intensivmed Notfmed. 107 (6): 448–53. doi:10.1007/s00063-012-0113-2. PMID 22878518. 
  7. ^ Wang, X; Liu, H; Chen, J; Huang, Y; Li, L; Rampersad, S; Qu, S (21 April 2016). "Metabolic Characteristics in Obese Patients Complicated by Mild Thyroid Hormone Deficiency.". Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 48: 331–7. doi:10.1055/s-0042-105150. PMID 27101096. 
  8. ^ Dietrich JW, Landgrafe G, Fotiadou EH (2012). "TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis". Journal of Thyroid Research. 2012: 351864. doi:10.1155/2012/351864. PMC 3544290Freely accessible. PMID 23365787. 
  9. ^ Rosolowska-Huszcz D, Kozlowska L, Rydzewski A (Aug 2005). "Influence of low protein diet on nonthyroidal illness syndrome in chronic renal failure". Endocrine. 27 (3): 283–8. doi:10.1385/endo:27:3:283. PMID 16230785. 
  10. ^ Liu S, Ren J, Zhao Y, Han G, Hong Z, Yan D, Chen J, Gu G, Wang G, Wang X, Fan C, Li J (2013). "Nonthyroidal Illness Syndrome: ist it Far Away From Crohn's Disease?". J Clin Gastroenterol. 47 (2): 153–9. doi:10.1097/MCG.0b013e318254ea8a. PMID 22874844. 
  11. ^ Hoermann, Rudolf; Midgley, John E.M.; Larisch, Rolf; Dietrich, Johannes W. (18 August 2016). "Relational Stability of Thyroid Hormones in Euthyroid Subjects and Patients with Autoimmune Thyroid Disease". European Thyroid Journal. 5: 171–179. doi:10.1159/000447967. PMC 5091265Freely accessible. PMID 27843807. 
  12. ^ Hoermann, Rudolf; Midgley, John E. M.; Larisch, Rolf; Dietrich, Johannes W. (7 November 2016). "Relational Stability in the Expression of Normality, Variation, and Control of Thyroid Function". Frontiers in Endocrinology. 7: 142. doi:10.3389/fendo.2016.00142. PMID 27872610. Retrieved 7 November 2016.